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Dissertations / Theses on the topic 'Epithelial-mesenchymal transition'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Qiao, Bin. "Epithelial-Mesenchymal Transition and Mesenchymal-Epithelial Transition in Oral Stem Cell Carcinogenesis." Thesis, Griffith University, 2011. http://hdl.handle.net/10072/367467.

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Oral squamous cell carcinoma (OSCC), derived from normal oral epithelium transformation, remains a major public health problem world-wide. The prognosis of OSCCs that occur on lips is good, while other sites of oral mucosa where OSCC appears are more progressive, invasive and metastatic. A small subset of cells within a malignant neoplasm, named cancer stem cells (CSCs) or tumour initiating cells are thought to be capable of initiating the neoplasm itself, and of driving its growth and recurrance after treatment. The precise origin of CSCs is an ambiguous issue at present. The first proposal o

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2

Robson, Ewan John Douglas. "Characterisation of epithelial-mesenchymal transition in murine mammary epithelial cells." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616130.

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3

Millanes, Romero Alba 1986. "Heterochromatin dynamics during epithelial-to-mesenchymal transition." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/129339.

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Although heterochromatin is enriched with repressive traits, it is actively transcribed, giving rise to large amounts of non-coding RNAs. These transcripts are responsible for the formation and maintenance of heterochromatin, but little is known about how their transcription is regulated. In this thesis we show that Snail1 transcription factor represses mouse pericentromeric transcription and regulates heterochromatin organization through the action of the H3K4 deaminase LOXL2. Snail1 has a key role in epithelial-to-mesenchymal transition (EMT). We show that, also during this process, Sn

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4

Tan, E.-Jean. "Transcriptional and Epigenetic Regulation of Epithelial-Mesenchymal Transition." Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-206120.

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The transforming growth factor beta (TGFβ) is a cytokine that regulates a plethora of cellular processes such as cell proliferation, differentiation, migration and apoptosis. TGFβ signals via serine/threonine kinase receptors and activates the Smads to regulate gene expression. Enigmatically, TGFβ has a dichotomous role as a tumor suppressor and a tumor promoter in cancer. At early stages of tumorigenesis, TGFβ acts as a tumor suppressor by exerting growth inhibitory effects and inducing apoptosis. However, at advanced stages, TGFβ contributes to tumor malignancy by promoting invasion and meta

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5

Cheung, Pak-yan, and 張柏欣. "Esophageal carcinogenesis: immortalization, transformation and epithelial-mesenchymal transition." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290379.

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6

Abdulla, Tariq. "Advances in modelling of epithelial to mesenchymal transition." Thesis, Loughborough University, 2013. https://dspace.lboro.ac.uk/2134/12744.

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Epithelial to Mesenchymal Transition (EMT) is a cellular transformation process that is employed repeatedly and ubiquitously during vertebrate morphogenesis to build complex tissues and organs. Cellular transformations that occur during cancer cell invasion are phenotypically similar to developmental EMT, and involve the same molecular signalling pathways. EMT processes are diverse, but are characterised by: a loss of cell-cell adhesion; a gain in cell-matrix adhesion; an increase in cell motility; the secretion of proteases that degrade basement membrane proteins; an increased resistance to a

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7

Cheung, Pak-yan. "Esophageal carcinogenesis : immortalization, transformation and epithelial-mesenchymal transition /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290379.

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8

De, Arpan. "Circadian clock regulation of epithelial-mesenchymal and mesenchymal-epithelial transitions in glioma and breast cancer cells." Bowling Green State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1566494866910786.

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9

Ilter, Didem. "The Role of ERK2 in Regulating Epithelial-Mesenchymal Transition." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11407.

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Epithelial-mesenchymal transition (EMT) is a fundamental developmental program, which is believed to be reactivated during the progression of in situ carcinoma to aggressive metastatic cancers. Ras-ERK pathway has been shown to play a crucial role in EMT. We have previously shown that ERK2, but not ERK1, is necessary for RasV12-induced EMT and overexpression of ERK2 is sufficient to promote EMT. ERK2 promotes EMT by regulating several factors, including the upregulation of transcription factors ZEB1/2. ZEB1/2 repress expression of E-cadherin, which is necessary for polar epithelial tissue form

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10

Dubois-Marshall, Sylvie. "Understanding epithelial to mesenchymal transition in human breast cancer." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/24541.

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Background and aims: Increasing evidence suggests that epithelial to mesenchymal transition (EMT) has a key role in breast cancer progression, underlying invasion, metastatic dissemination and acquisition of therapeutic resistance. However, this role is predominantly inferred from in vitro and animal studies and controversy regarding EMT in human cancer remains. This thesis has two principle aims. Firstly, to clarify the role of EMT in human breast cancer at the protein level. Secondly, to develop a three-dimensional in vitro assay to investigate cell invasion. Experimental Design: Two indepen

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11

Pellarin, Ilenia. "HMGA PROTEINS IN EPITHELIAL-MESENCHYMAL TRANSITION AND TUMOUR PROGRESSION." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10117.

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2012/2013<br>High Mobility Group A (HMGA1a, HMGA1b and HMGA2) proteins are architectural nuclear factors, physiological expressed during embryonic development and re-expressed at high levels following neoplastic transformation, playing essential functions in both these processes thanks to their particular plasticity and consequently multifunctionality. HMGA are involved in a wide number of cellular processes, including Epithelial-Mesenchymal transition (EMT), a biologic developmental process characterized by the conversion of epithelial cells to motile mesenchymal ones, with increased capacity

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12

Porta, de la Riva Montserrat. "Transcriptional activation induced by snail 1 during epithelial-mesenchymal transition." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7205.

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La transició epiteli-mesènquima (TEM) és un procés en què cèl lules epitelials, immòbils i amb polaritat apico-basal transiten cap un fenotip mesenquimal o fibroblàstic. L'expressió del factor de transcripció snail1 és suficient per induir TEM en cèl lules en cultiu i és necessari per la majoria de les TEM fisiològiques descrites. Snail1 és un membre de la família de proteïnes amb dits de Zinc que reprimeix gens epitelials (com l'E-cadherina) a través de la unió directa a seqüències especifiques dels promotors anomenades caixes E i posterior reclutament de corepressors. La TEM també es caracte

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13

Chandler, Heather Lynn. "Epithelial-mesenchymal transition in the anterior segment of the eye." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1154533588.

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14

Rygiel, Karolina Anna. "Epithelial to mesenchymal transition : a possible route to liver fibrogenesis." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506551.

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15

Perera, Nirmal. "The role of YAP 1 in regulating epithelial-mesenchymal transition." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10024780/.

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The Yes-associated protein 1 (YAP1) is an oncogenic transcriptional co-activator, which is negatively regulated by the Hippo signalling pathway. If the Hippo pathway is deregulated, YAP1 can translocate to the nucleus where it interacts with various transcription factors to drive transcription. Suppressing YAP1 as a therapeutic strategy has attracted considerable interest, especially since YAP1 and oncogenic RAS have been shown to interact in different tumour models. I evaluated the role(s) of YAP1 in transforming non-tumourigenic epithelial cells along the epithelial-mesenchymal transition (E

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16

Kah, Kong Jie. "ZEB1 is a central mediator of the Epithelial-Mesenchymal Transition." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/72930.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2012.<br>Vita. Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>Carcinomas are solid tumors arising from epithelial tissue, and account for the majority of cancer deaths in the United States. In most occurrences of carcinoma, it is the metastases that kill, not the primary tumor. The Epithelial-Mesenchymal Transition (EMT) provides a model by which tightly associated epithelial cancer cells can disseminate to distant sites. Many factors are known to trigger the EMT, but the extent to which

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17

Hussey, George S. "Identification of a Post-Transcriptional Mechanism Regulating Epithelial-Mesenchymal Transition." Cleveland State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=csu1354051158.

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18

Kim, Taewan. "The function of microRNAs in p53-regulated epithelial-mesenchymal transition." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1322493623.

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19

Nakajima, Sanae. "N-cadherin expression and epithelial mesenchymal transition in pancreatic carcinoma." Kyoto University, 2007. http://hdl.handle.net/2433/135910.

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20

Bozić, Stanojević Milica. "Glutamatergic signaling in proximal tubular cells maintains the epithelial phenotype and decreases epithelial-mesenchymal transition." Doctoral thesis, Universitat de Lleida, 2011. http://hdl.handle.net/10803/51013.

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21

Monsor, Rehanna. "The role of the IGF axis in epithelial to mesenchymal transition in prostate epithelial cells." Thesis, University of Bristol, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723508.

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22

Gorowiec, Marta Roksana. "The role of oxidative stress in lung epithelial cells undergoing epithelial-to-mesenchymal transition (EMT)." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512043.

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23

Abdulkareem, Ali Abbas. "Potential involvement of epithelial-mesenchymal transition in the pathogenesis of periodontitis." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7340/.

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Epithelial-mesenchymal transition is reportedly important in loss of epithelial integrity and cell migration in inflammatory/infectious diseases and cancer. Since Gram negative anaerobic periodontal pathogens are well-recognized to induce intense inflammatory responses; the present study investigated their ability to induce EMT in vitro. A 2D chronic inflammatory model was developed using either the H400 oral keratinocyte cell-line or primary rat oral keratinocytes which were exposed to heat-killed Fusobacterium nucleatum, Porphyromonas gingivalis and Escherichia coli LPS for up to 8-days. EMT

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24

Jager, Michal. "The role of aortic carboxypeptidase-like protein in epithelial-mesenchymal transition." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12428.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Communication from stromal cells to tumors contributes to the progression of several carcinomas. Stromal fibroblasts, also referred to as cancer associated fibroblasts, in part through their production of secret

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25

Han, ShuYi. "Histone variant H2A.Z : a master regulator of epithelial-to-mesenchymal transition." Phd thesis, Canberra, ACT : The Australian National University, 2014. http://hdl.handle.net/1885/151759.

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26

Stylianou, Nataly. "Investigating the role of the epithelial-mesenchymal plasticity in prostate cancer." Thesis, Queensland University of Technology, 2017. https://eprints.qut.edu.au/107979/1/Nataly_Stylianou_Thesis.pdf.

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This thesis was a step forward in better understanding the involvement of cancer cell plasticity in the progression of prostate cancer to aggressive disease. These studies described for the first time the transcriptional landscape of epithelial-mesenchymal plasticity in prostate cancer which led to the discovery of a molecular signature capable of identifying high-risk patients. In addition, this project revealed new-found molecular targets that may regulate cancer cell plasticity, thus making them attractive therapeutic options for patients with prostate cancer.

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27

Scott, Lewis. "Mechanochemical Regulation of Epithelial Tissue Remodeling: A Multiscale Computational Model of the Epithelial-Mesenchymal Transition Program." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/6032.

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Epithelial-mesenchymal transition (EMT) regulates the cellular processes of migration, growth, and proliferation - as well as the collective cellular process of tissue remodeling - in response to mechanical and chemical stimuli in the cellular microenvironment. Cells of the epithelium form cell-cell junctions with adjacent cells to function as a barrier between the body and its environment. By distributing localized stress throughout the tissue, this mechanical coupling between cells maintains tensional homeostasis in epithelial tissue structures and provides positional information for regulat

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28

Laffin, Brian Edward. "Regulation of epithelial-mesenchymal transition and DNA damage responses by singleminded-2s." [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-3076.

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29

Tse, Gina Chan. "The role of epithelial mesenchymal transition transcription factors on DNA damage response." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/38292.

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The role of epithelial mesenchymal transition (EMT) has been identified to influence many processes associated with cancer development; malignant transformation, invasion, resistance to therapeutics to name but a few. Despite this, little is known about the relationship between EMT and DNA damage response (DDR). This study aims to investigate how the EMT programs activated in different cancer cell backgrounds influence DDR. The understanding of this interrelationship will help in designing new therapies to combat forms of cancer in which EMT plays a role. Microarray data obtained in three diff

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30

Cummings, Natalie Marie. "The role of epithelial mesenchymal transition in the progression of bronchial dysplasia." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607647.

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31

Volakis, Leonithas I. "Evaluating Dynamic Changes in Cancer Cell Mechanics during Epithelial to Mesenchymal Transition." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492739871307445.

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32

Block, C. James Garnet. "Investigation of the Common Epithelial-to-Mesenchymal Transition Program in Breast Cancer." Thesis, Wayne State University, 2022. http://pqdtopen.proquest.com/#viewpdf?dispub=27741360.

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The epithelial-to-mesenchymal transition (EMT) is a critical mechanism during the process of normal embryonic development and wound healing that can be pathologically re-activated during cancer progression. We hypothesized that comparing the transcriptional programs of multiple EMT-driving transcription factors (EMT-TFs) would identify a common set of critical EMT effectors. After elucidating this common transcriptional program, the commonly upregulated RNA binding protein RBMS3 was chosen as a target for functional validation. RBMS3 was both necessary and sufficient for EMT and breast cancer

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33

Rao, Srinivasa Rao. "Novel signalling pathways regulating epithelial-mesenchymal transition in bone metastatic prostate cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:bc90d3e0-420c-424f-b6ea-5567cbb21529.

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Prostate cancer (PCa) cells predominantly metastasize to bone and the complex crosstalk between PCa cells and osteoblasts (bone-forming cells) and osteoclasts (bone-destroying cells) leads to increased tumour growth and worsening of bone disease. Understanding the mechanisms of PCa bone metastasis can identify the aggressive fraction of PCa resulting in earlier intervention. The ability of PCa cells to express bone cell-specific features, termed osteomimicry, could potentially explain the osteotropic nature of PCa cells. The aim of this study was to determine the role of osteomimicry in the re

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34

Scholtes, Ben [Verfasser], and Gernot [Akademischer Betreuer] Zissel. "CCL18 als Induktor der "Epithelial to Mesenchymal Transition" im nicht-kleinzelligen Lungenkarzinom." Freiburg : Universität, 2013. http://d-nb.info/1123478201/34.

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35

Zhai, Yubo. "REDEFINING THE MOLECULAR BASIS OF EPITHELIAL MESENCHYMAL TRANSITION IN BREAST CANCER METASTASIS." Master's thesis, Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/216586.

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Biochemistry<br>M.S.<br>Metastasis is a multi-step process that begins with cancer cells migrating and invading away from the primary tumor site and extravasating into distant organs to establish a secondary tumor. The loss of epithelial expression markers by neoplastic breast cancer cells in the primary tumor is believed to play a pivotal role during breast cancer metastasis. This phenomenon is the hallmark of the epithelial mesenchymal transition (EMT) process. Gene expression microarrays were performed to investigate key functional elements on an in vitro metastasis model derived from human

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36

Griggs, Lauren. "FIBRONECTIN MECHANICS AND SIGNALING IN TGF-β1-INDUCED EPITHELIAL TO MESENCHYMAL TRANSITION". VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5539.

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Epithelial to Mesenchymal Transition (EMT) is a dynamic process by which a distinct change in the phenotype and function of epithelial cells render them as mesenchymal cells. Characteristics of mesenchymal cells include the ability to invade, increased migratory kinetics and heightened resistance to apoptosis. Therefore, there is a strong need to fully understand the mechanism for the induction of EMT in pathological conditions such as carcinoma progression. Recent advances highlight two pivotal contributors, soluble growth factor (gf) signals, and mechanical signals, in the process. However,

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37

Upadhyaya, Akanksha. "Targeting epithelial to mesenchymal transition (EMT) to modulate prostate cancer cell chemoresistance." Thesis, Queensland University of Technology, 2020. https://eprints.qut.edu.au/201657/1/Akanksha_Upadhyaya_Thesis.pdf.

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Understanding why some cancer cells do not respond to chemotherapy is critical to developing new ways to control cancer. This project defined the important role of tumour cell plasticity in the response of prostate cancer cells to chemotherapy drugs. Key proteins that control cell plasticity have emerged as promising theranostic targets that can be pursued to develop new approaches to improve outcomes for men with metastatic prostate cancer.

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38

Ran, Ran. "RUNX transcription factors drive epithelial to mesenchymal transition in metastatic breast cancer cells." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/runx-transcription-factors-drive-epithelial-to-mesenchymal-transition-in-metastatic-breast-cancer-cells(224fac5a-0188-4dd5-8c20-b1749fbbc32d).html.

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In the UK, 12,000 patients die from metastatic breast cancer annually. There is therefore an urgent need to identify the molecules that cause metastasis. Recent work has revealed a role for the RUNX family of transcription factors in the development of metastatic breast cancer. The RUNX proteins form active transcription factor complexes when bound by the heterodimeric partner CBFβ to regulate the expression of metastatic genes. Previous work from our laboratory has demonstrated that knockdown of CBFβ resulted in a decreased invasion capacity of the metastatic breast cancer cell line MDA-MB-23

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39

Zhu, Menglei. "FUNCTION OF ANDROGEN RECEPTOR IN PROSTATE CANCER EPITHELIAL MESENCHYMAL TRANSITION AND MICROTUBULE TARGETING." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/109.

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Prostate cancer is the most frequently diagnosed non-skin cancer and the third leading cause of cancer mortality among men in the US. Androgens are functionally required for the normal growth of the prostate gland and play a critical role in prostate tumor development and progression. Epithelial-mesenchymal-transition (EMT) is an important process during normal development, and cancer cell metastasis. This study examined the ability of androgens to influence EMT of prostate cancer epithelial cells and evaluate the effect of taxol chemotherapy on androgen signaling in prostate cancer cells in p

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40

Hamilton, Julie Anne. "Targeting epithelial-to-mesenchymal transition (EMT) in feline oral squamous cell carcinoma (FOSCC)." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31357.

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Squamous cell carcinoma of the head and neck (HNSCC) is an extremely common and devastating disease with a bleak prognosis. Despite intensive research, survival rates have not improved over the past 30 years principally due to untreatable recurrent/metastasising disease. Feline oral squamous cell carcinoma (FOSCC) is an equally common disease in cats with an even less favourable prognosis than humans. Human and feline squamous cell carcinomas share similar etiopathogenesis, molecular markers, tumour biology and treatment thus making FOSCC an excellent model for HNSCC. Epithelial to mesenchymal

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41

Jaca, Anelisa. "Investigating the relationship between miRNA expression and epithelial mesenchymal transition in colorectal cancer." Doctoral thesis, University of Cape Town, 2016. http://hdl.handle.net/11427/23041.

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Introduction: Epithelial-mesenchymal transition (EMT) is characterized by the loss of an epithelial phenotype and gain of a mesenchymal phenotype, i.e., migratory and metastatic properties. The EMT process is therefore characterized by a low expression of E-cadherin and high expression of mesenchymal markers (e.g., N-cadherin, snail and vimentin). It is stated that cells which have undergone EMT also gain stem cell features. Therefore, both EMT and stem cell phenotypes have been implicated in carcinogenesis and metastasis of tumour cells. Furthermore, EMT is regulated by small non-coding molec

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42

Beach, Jordan R. "Roles and Regulation of Nonmuscle Myosin II During Cytokinesis and Epithelial-Mesenchymal Transition." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1323099118.

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43

Chou, Chih-Chien. "Inhibition of Epithelial-to-Mesenchymal Transition by Anti-tumor Agents in Cancer Cells." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396875461.

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Bhangu, Aneel. "Epithelial mesenchymal transition and resistance to neoadjuvant radiotherapy in locally advanced rectal cancer." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24734.

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Background: Non-response to neoadjuvant therapy is a significant challenge for clinicians managing solid cancers. This thesis aimed to determine whether Epithelial Mesenchymal Transition (EMT) was associated with non-response to neoadjuvant therapy in patients with locally advanced rectal cancer. Methods: Representative tissue specimens from the tumour invasive front of consecutive patients undergoing resection of rectal cancer from 2009-2011 were used. Patients with marked regression to neoadjuvant therapy were classified as responders with the remainder as non-responders. Markers of EMT incl

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Espineda, Cromwell Eneria. "Analysis of Na,K-ATPase function and expression during epithelial to mesenchymal transition." Diss., Restricted to subscribing institutions, 2005. http://proquest.umi.com/pqdweb?did=888866071&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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46

Mei-YiLee and 李美逸. "Epithelial-Mesenchymal Transition in Cervical Cancer." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/15523118454688668198.

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47

Pais, Ricardo Jorge Fonseca Tavares Godinho. "How cells initiate Epithelial-to-Mesenchymal Transition?" Doctoral thesis, 2018. http://hdl.handle.net/10362/61583.

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"Over the last decade, Epithelial-to-Mesenchymal Transition (EMT) has gained the attention of cancer researchers due to its potential to promote cancer migration and metastasis. However, the complexity of EMT intertwined regulation and the involvement of multiple signals in the tumour microenvironment have been limiting the understanding of how this process can be controlled. Cell-cell adhesion and focal adhesion dynamics are two critical properties that change during EMT, which provide a simple way to characterize distinct modes of cancer migration. Therefore, the main focus of this th

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48

Keitel, Ulrike. "Attenuated apoptosis as consequence of Epithelial Mesenchymal Transition." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0022-5F50-4.

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49

"The role of CFTR in epithelial-mesenchymal transition." 2012. http://library.cuhk.edu.hk/record=b5549646.

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上皮間充質轉化（EMT），作為重要的生理和病理事件，廣泛的參與胚胎發育、組織纖維化病變及腫瘤轉移的過程。這一顯著的細胞表型變化包括上皮細胞失去緊密連接和極性，上皮細胞呈現纖維細胞形態以及增強的細胞移動性。囊性纖維變性跨膜電導調節器（CFTR）是一種廣泛表達於上皮細胞的氯離子和碳酸根離子通道。研究證實，CFTR 的蛋白轉運與上皮連接的形成和功能有關，同時 CFTR 的表達受到 EMT 誘導因子 HIF-1 和 TGF-β 的反向調節。另外，CFTR 的表達和功能被證實參與 EMT 相關信號分子 Wnt 和 NF-κB活性的調節。基於上述發現，本研究旨在闡述 CFTR 與 EMT 的相關性。<br>CFTR 參與的腎上皮 EMT 以及後續的腎纖維化首先被關注。實驗表明，在腎上皮細胞（MDCK）中，小 RNA 介導的 CFTR 基因敲降或抑製劑引起的CFTR 通道功能缺陷均引起間充質細胞特徵的出現，包括纖維狀細胞形態、細胞連接分子 E-cadherin, ZO-1 和 Occludin 表達下調和間充質細胞標誌分子 Vimentin 和 N-cadherin 上調、上皮細胞跨膜電阻減低以及細胞遷徙能力的增強。有趣的是，在單側尿道結紮的腎纖維化模型中，CFTR 表達被顯著下調。同時，動物實驗證實一個最常見的 CFTR 分子突變（deltaF508 -/-）增加了單側尿道結紮導致的腎纖維化的

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Su, Chun-Wei, and 蘇俊維. "The Role of AMPK in Epithelial-Mesenchymal Transition." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/85946232153224139416.

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碩士<br>國立臺灣大學<br>藥理學研究所<br>97<br>AMPK is a serine/threonine protein kinase that serves as an energy sensor in all eukaryoic cells, regulating energy balance. Epithelial-Mesenchymal Transition (EMT) is a crucial process for cancer cells to acquire invasive and metastatic phenotype. Loss of E-cadherin is a hallmark of EMT. Thus, re-expression of E-cadherin could elicit inverse process Mesenchymal-Epithelial Transition (MET). In lung adenocarcinomas, TGF-β is a major inducer of EMT. In this study, we found that AMPK activators AICAR and 2-DG downregulated E-cadherin expression, while AMPK inhibito

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